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AP® Biology flashcards Biology 101 flashcards
1
Q

What are the 4 steps in normal wound healing?

A
  1. Haemostasis
  2. Inflammation
  3. New tissue formation
  4. Tissue remodelling
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2
Q

What are the 5 steps in haemostasis and what is its effect?

A
  1. Release of collagen and von Willebrand factors
  2. Platelets adhere to collagen
  3. Release thromboxane
  4. Begin to aggregate together
  5. Bind to fibrinogen which is converted to a fibrin mesh
    = Platelet plug restoring physical barrier
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3
Q

What are the 5 steps in inflammation?

A
  1. Release of pro-inflammatory cytokines (prostaglandins, histamine and thromboxane)
  2. Increased permeability of vessels and recruitment of neutrophils
  3. Activation of complement and macrophages
  4. Macrophages stimulate angiogenesis and re-epithelialization
  5. T and B cells are recruited
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4
Q

What are the 5 steps in new tissue formation?

A
  1. Fibroblast migration and production of collagen
  2. Other epithelial cells are attracts
  3. Angiogenesis occurs due to VEGF
  4. Re-epithelialization by basal keratinocytes
  5. Reoganisation by collagenases and metalloproteinases
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5
Q

What 2 things occur in tissue remodelling?

A
  1. Collagen remodelling
    - Switch Type III for Type I which is stronger and has more cross-links
  2. Vascular maturation
    - Apoptosis of old vessels that are no longer required
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6
Q

How does Human Papilloma Virus (HPV) avoid the host immune system?

A
  1. Doesn’t express viral proteins until inflammation has decreased
  2. Rapid infection to avoid detection
  3. Infects reservoirs in basal cells
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7
Q

How does HPV evade the immune system, what proteins are involved?

A

E6
- Disrupts interferon signalling by interfering with Tyk2
E7
- Disrupts STAT signalling
- Suppresses Interferon response factor 1 (IRF1)
- Prevents presentation of antigen on MHC
E5
- Reduces conc of MHC

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8
Q

What are the pathological effects of the HPV proteins E6 and E7?

A

E6
- Suppresses p53, causes continuous cell cycling
- Inhibits differentiation by inhibiting NOTCH signalling
E7
- Binds to retinoblastoma, drives cell cycle

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9
Q

What are the two types of HPV?

A

Low risk
- Causes benign lesions
- Slight suppression of signalling
- e.g. HPV6, HPV11
High risk
- Causes lesions that can undergo neoplasia into cancer
- Aggressive suppression of signalling such as NOTCH
- e.g. HPV16, HPV18

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10
Q

What is NOTCH signalling? And what are its roles? (4)

A
  1. NOTCH receptor is transmembrane and can be bound to
  2. Binding causes release of intracellular domain
  3. Activates transcription and regulates expression
    Roles
    - Cell fate determination
    - Maintaining stem cell population
    - Regulates T cell development and differentiation
    - Involves in angiogenesis
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11
Q

How does the immune system persist with and eventually clear HPV infections?

A

Persistence
- due to low HPV gene expression levels
- E6 produces E-cadherin which reduces retention of Langerhan cells (DC) in the epithelium for detection
Clearance
- Activation of T cell immunity

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12
Q

Describe the vaccine against HPV

A
  • Recombinant vaccine
  • Mixed with an adjuvant
  • Mix of viral coat proteins
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13
Q

What are the steps in the pathology of Hepatitis B?

A
  1. Cytokines such as TNF-α and IL-6 are produced
  2. Activation of Nf-kB, causes resistance against apoptosis
  3. Production of ROS
  4. Chronic inflammation and tissue remodelling
    = Liver cirrhosis and Hepatocellular cancer
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14
Q

What are the steps in the pathology of H. pylori?

A
  1. Entry into the mucosal layer
  2. Secretion of mucinase, makes mucus less viscous
  3. Attach via BabA and BabB surface adhesins
  4. Secretes CagA pathogenicity island
    - Cells lose polarity and junctions disrupted
  5. VacA can be released causing pore formation
  6. Results in apoptosis
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15
Q

What is dysplasia and how is it different to carcinoma?

A

Dysplasia - changes in cell morphology. Doesn’t invade the basement membrane

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16
Q

What is immunosuppression?

A

When the host immune system activity is decreased

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17
Q

How do carcinomas and sarcomas differ?

A

Carcinoma - epithelial
Sarcoma - mesenchyme e.g. endothelial

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18
Q

What are the two differing types of immunosuppression?

A
  1. Congenital (genetic) v acquired
  2. Innate v adaptive
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19
Q

What treatments are the for autoimmunity?

A

NSAIDs (non-steroidal anti-inflammatory)
- Cell cycle inhibitors
- Anti-TNF e.g. infliximab
- Cyclosporin

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20
Q

What are the two ways in which immunosuppression can cause cancer?

A
  1. Lack of viral control
  2. Inability to respond to antigens, decreased MHC
21
Q

List 5 examples of immunosuppression-related cancers

A
  1. UV-induced cancers
  2. Merkel cell carcinoma
  3. Burkitt lymphoma
  4. Kaposi’s sarcoma
  5. HPV driven anogenital carcinoma
22
Q

How does UV-induced carcinoma develop?

A
  1. UV mutates keratinocyte DNA
  2. Causes increased production of IL-10
  3. IL-10 acts as an anti- inflammatory cytokine
23
Q

How does Merkel cell carcinoma develop?

A

Infection with merkel cell polyomavirus
- T region that becomes truncated can inhibit Rb and promote cell division

24
Q

How does HPV driven anogential carcinoma develop?

A
  • HPV infection releases E6 and E7
  • E6 and E7 target p53, Rb and NOTCH signalling, causing carcinoma
  • HPV only infects epithelial cells
  • Immunosuppressed patients, mainly develop cancers in the anogenital region
25
Q

How does Burkitt lymphoma develop?

A

Infection with EBV (HHV-4 , a herpes virus)
Targets B cells and leads to rapid proliferation
Detection: Mib1 staining

26
Q

What are the different variants of EBV and their effect on lymphoma development?

A

Endemic: Africa
- Develop in the midline
Sporadic + Immunocompromised related
- Develop in the abdominal region

27
Q

What is the cause for Kaposi’s sarcoma?

A

HHV-8 (herpes)
- Encodes LANA1 oncogene
- Disrupts signalling (NOTCH, JAK/STAT)
- Promotes anti-apoptosis
- Disrupts Rb and p53

28
Q

What are the 3 physical layers of defence in the foetus?

A
  1. Placenta
  2. Amniotic fluid
    - antimicrobial proteins
  3. Cervical plug
29
Q

What are the 4 sources of haematopoietic stem cells?

A
  1. Yolk sac
    - Primitive wave
  2. Aorta-gonad mesonephros
  3. Liver
  4. Bone marrow
30
Q

What is the difference between primitive and definitive haematopoietis?

A

Primitive - only macrophages, RBC, megakaryocytes
RBC- retain nuclei
Definitive - all cells, RBC etc.

31
Q

What prevents maternal and foetal cells from attacking each other upon recognition? Give an example of this response against maternal antigens.

A

Foetal DC or T cell cause development of Treg, instead of pro-inflammatory
Evidence:
Group with maternal antigens experienced a higher early rejection rate, mismatch with of maternal HLA antigen better than mismatch of paternal antigens from sibling
- Burlingham et al., 1998

32
Q

What are the properties of Treg cells? How are can these be identified?

A

FOXP3 and CD25
Analysed by flow cytometry

33
Q

What are the 4 components of neonate immunology?

A
  1. Arginase
  2. Maternal IgG
  3. Breast milk - IgA
  4. Vaccination
34
Q

What is the role arginase?

A

Breaks down L-arginine
Molecule required by T cells to form TNF-α

35
Q

How are maternal IgG transported across the placenta?

A

Presentation of FcRn
Endocytosed and acidified
- Occurs in second trimester
e.g. against Bordetella pertussis

36
Q

What are the components found in breast milk?

A

IgA - helps protect from GIT
Lactoferrin- reduces iron, which bacteria require
Lysosyme - antimicrobial, disrupting cell wall

37
Q

Describe the pathology and treatment associated with Bordetella pertussis (Whooping cough)

A

Highly infectious
Severe cough
Treatment
- Vaccination of mother, so that IgG are transferred

38
Q

What is rhesus disease? How can it be treated?

A
  • Caused when mother is Rh -ve and foetus is Rh +ve
  • Occurs when maternal and foetal blood mix during parturition
  • Injection of IgD, which will bind to foetal RBC and prevent detection
39
Q

Why does susceptibility to different pathogens vary in the foetus ?

A

Different antibodies are transferred across with different levels of efficiency
Measles - 100%
SARS- Cov2 less efficient

40
Q

What are developing therapies for genetic disease in utero?

A
  1. In utero transplantation
    - Doesn’t work against all diseases
    - Prevents excessive damage
    - Good against osteogenesis imperfecta, SCID
  2. In utero gene therapy
    - extract and culture cells
41
Q

What is the cause for SCID and what is its pathology?

A

Mutation in CD132
Cause lack of T and NK cells

42
Q

Compare and contrast solid and liquid neoplasms

A
  1. Invasiveness
    - Harder to tell in liquid cancers
  2. Density dependent growth
    - Stromal cell not necessary in liquid cancers
  3. Morphology
    - Benign and lymphoma similar looking in liquid cancers
  4. Translocations
    - More translocations in haematopoietic cancers, due to VDJ recombination common for switching in chromosome 14
43
Q

What are 5 steps in diagnosis of haematopoietic cancers?

A
  1. Morphology inspection
  2. Flow cytometry
  3. Clonality studies
  4. Molecular genetics
  5. WHO classification
44
Q

What is the difference between low and high grade lymphoma?

A

Low grade - smaller cells
High grade - larger cells

45
Q

What are the 3 key sites for the development of lymphoid neoplasia?

A
  1. lymph nodes
  2. Spleen/ thymus
  3. Mucosal associated lymphoid tissue (MALT)
46
Q

What are the 3 main causes of lymphoma?

A
  1. Translocation driven
    - Follicular lymphoma chromosome 14 and 18 swap = Bcl-2 and CD10 presentation
  2. Antigen driven
    - Antigen promotes translocation e.g. H.pylori activates Nf-kB
  3. Point mutation driven
    - Rare, but single mutation can activate BRAF V600E in Hairy Cell Leukaemia
47
Q

What are the 3 methods for immunotherapy?

A
  1. Target checkpoint
    - Prevent checkpoint, cause constant activation of T cells via Ab against CTLA4 (Ipilimumab) and PD1/ PD-L1
  2. Adoptive T cell therapies
    - Harvest T cells then reinfuse
  3. Engineered adoptive T cells
    - CAR T cells, against CD19 on B cells
48
Q

What is the role of RIG-I?

A

Cytoplasmic receptor detecting viral RNA and signals via Nf-kB and IRF3

Biology of Disease (4 decks)

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